Engineered Tissues to Quantify Collective Cell Migration During Morphogenesis

Manivannan, Sriram; Gleghorn, Jason P.; Nelson, Celeste M.

doi:10.1007/978-1-61779-851-1_16

Cited by 7 publications

(6 citation statements)

References 16 publications

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“…A reductionist approach to 3D models, the use of immortalized cells including Madin-Darby canine kidney cells (MDCK) and kidney proximal tubule cells (LLC-PK1) in a 3D matrix, has significantly contributed to our understanding of the pathology of ADPKD. Grantham and colleagues (18,25) introduced the 3D MDCK model system as a foundational tool for the study of ADPKD cystogenesis with their studies on determinants of fluid secretion. The MDCK 3D culture system shared characteristics with the distal nephron, including being responsive to the addition of cAMP agonists (4,18,44).…”

Section: Immortalized Cell Models Are Useful As Proliferation and Flumentioning

confidence: 99%

Three-dimensional in vitro models answer the right questions in ADPKD cystogenesis

Dixon

Woodward

2018

American Journal of Physiology-Renal Physiology

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Novel technologies, new understanding of the basement membrane composition, and better comprehension of the embryonic development of the mammalian kidney have led to explosive growth in the use of three-dimensional in vitro models to study a range of human disease pathologies (Clevers H. Cell 165: 1586-1597, 2016; Shamir ER, Ewald AJ. Nat Rev Mol Cell Biol 15: 647-664, 2014). The development of these effective model systems represents a new tool to study the progressive cystogenesis of autosomal dominant polycystic kidney disease (ADPKD). ADPKD is a prevalent and complex monogenetic disease, characterized by the pathological formation of fluid fill cysts in renal tissue (Grantham JJ, Mulamalla S, Swenson-Fields KI. Nat Rev Nephrol 7: 556-566, 2011; Takiar V, Caplan MJ. Biochim Biophys Acta 1812: 1337-1343, 2011). ADPKD cystogenesis is attributed to loss of function mutations in either PKD1 or PKD2, which encode for two transmembrane proteins, polycystin-1 and polycystin-2, and progresses with loss of both copies of either gene through a proposed two-hit mechanism with secondary somatic mutations (Delmas P, Padilla F, Osorio N, Coste B, Raoux M, Crest M. Biochem Biophys Res Commun 322: 1374-1383, 2004; Pei Y, Watnick T, He N, Wang K, Liang Y, Parfrey P, Germino G, St George-Hyslop P. Am Soc Nephrol 10: 1524-1529, 1999; Wu G, D'Agati V, Cai Y, Markowitz G, Park JH, Reynolds DM, Maeda Y, Le TC, Hou H Jr, Kucherlapati R, Edelmann W, Somlo S. Cell 93: 177-188, 1998). The exaggerated consequences of large fluid filled cysts result in fibrosis and nephron injury, leading initially to functional compensation but ultimately to dysfunction (Grantham JJ. Am J Kidney Dis 28: 788-803, 1996; Norman J. Biochim Biophys Acta 1812: 1327-1336, 2011; Song CJ, Zimmerman KA, Henke SJ, Yoder BK. Results Probl Cell Differ 60: 323-344, 2017). The complicated disease progression has scattered focus and resources across the spectrum of ADPKD research.

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Section: Immortalized Cell Models Are Useful As Proliferation and Flumentioning

confidence: 99%

Three-dimensional in vitro models answer the right questions in ADPKD cystogenesis

Dixon

Woodward

2018

American Journal of Physiology-Renal Physiology

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“…Replica micromolding can be used to produce 3D substrata within gels of ECM protein (Figure 3B) [56,107,128,129]. As with microcontact printing, this method uses silicone stamps with surface features defined via photolithography.…”

Section: Designing Microfabricated Tissues To Study Traction Forcesmentioning

confidence: 99%

Microfabricated tissues for investigating traction forces involved in cell migration and tissue morphogenesis

Nerger

Siedlik

Nelson

2016

Cell. Mol. Life Sci.

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Cell-generated forces drive an array of biological processes ranging from wound healing to tumor metastasis. Whereas experimental techniques such as traction force microscopy are capable of quantifying traction forces in multidimensional systems, the physical mechanisms by which these forces induce changes in tissue form remain to be elucidated. Understanding these mechanisms will ultimately require techniques that are capable of quantifying traction forces with high precision and accuracy in vivo or in systems that recapitulate in vivo conditions, such as microfabricated tissues and engineered substrata. To that end, here we review the fundamentals of traction forces, their quantification, and the use of microfabricated tissues designed to study these forces during cell migration and tissue morphogenesis. We emphasize the differences between traction forces in two- and three-dimensional systems, and highlight recently developed techniques for quantifying traction forces.

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“…This is critical as it correctly mimics the polarity of cells in vivo and indicates correct contact orientation with the extracellular matrix (ECM). These cells branch and migrate into collagen I hydrogel in the presence of hepatocyte growth factor (HGF) [42], are used to study the mechanisms involved in polycystic kidney disease [43,44], and have been utilized to study ifosfamide induced nephrotoxicity in microfluidic devices [45,46]. However, these cells are a heterogeneous population of kidney epithelial cells, they are not of human origin, and they do not have the same phenotype in 3D tissue culture as human renal PTC [47].…”

Section: Engineering Strategiesmentioning

confidence: 99%

“…Manivannan et al patterned collagen type I into channels using polydimethylsiloxane (PDMS) molds. These channels were then seeded with MDCK cells and covered with a collagen type I lid [42]. This system enabled controlled tubule formation and allowed the tracking of cell migration in 3D.…”

Section: Engineering Strategiesmentioning

confidence: 99%

Tissue-engineered kidney disease models

DesRochers

Palma

Kaplan

2014

Advanced Drug Delivery Reviews

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Renal disease represents a major health problem that often results in end-stage renal failure necessitating dialysis and eventually transplantation. Historically these diseases have been studied with patient observation and screening, animal models, and two-dimensional cell culture. In this review, we focus on recent advances in tissue engineered kidney disease models that have the capacity to compensate for the limitations of traditional modalities. The cells and materials utilized to develop these models are discussed and tissue engineered models of polycystic kidney disease, drug-induced nephrotoxicity, and the glomerulus are examined in detail. The application of these models has the potential to direct future disease treatments and preclinical drug development.

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Engineered Tissues to Quantify Collective Cell Migration During Morphogenesis

Cited by 7 publications

References 16 publications

Three-dimensional in vitro models answer the right questions in ADPKD cystogenesis

Three-dimensional in vitro models answer the right questions in ADPKD cystogenesis

Microfabricated tissues for investigating traction forces involved in cell migration and tissue morphogenesis

Tissue-engineered kidney disease models

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